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三氧化二砷与辐射的协同作用：触发细胞凋亡的内在途径

Synergistic Effects of Arsenic Trioxide and Radiation: Triggering the Intrinsic Pathway of Apoptosis.

作者信息

Moloudi Kave, Neshasteriz Ali, Hosseini Arshad, Eyvazzadeh Nazila, Shomali Mehdi, Eynali Samira, Mirzaei Elahe, Azarnezhad Asaad

机构信息

Radiation Sciences Department, Faculty of allied Medicine school, Iran University of Medical Sciences, Tehran, Iran.

Radiation biology research center, Iran University of medical sciences, Tehran, Iran.

出版信息

Iran Biomed J. 2017 Sep;21(5):330-7. doi: 10.18869/acadpub.ibj.21.5.330. Epub 2017 May 1.

DOI:10.18869/acadpub.ibj.21.5.330
PMID:28459147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5548965/
Abstract

BACKGROUND

Arsenic trioxide (ATO) has been reported as an effective anti-cancer and a US Food and Drug Administration (FDA) approved drug for treatment of some cancers. The aim of this study was to determine the underlying apoptosis molecular and cellular mechanisms of ATO in the presence or absence of ionizing radiation (IR) in vitro in the glioblastoma multiforme (GBM) cell line, U87MG.

METHODS

Cells were treated by different concentrations of ATO either in presence or absence of IR. Viability and apoptosis pathway of both treated and control groups were evaluated using MTT assay and the expression analysis of Bax, Bcl-2, and caspase-3 genes, respectively. All treatments were performed on 100-μm diameter spheroids.

RESULTS

Results showed a significant reduction in the survival of the cells in all treated groups. As expected, cell survival was much less in combination treatment than treatment with only ATO. Moreover, combination therapy made Bax and caspase-3 up-regulated and Bcl-2 down-regulated.

CONCLUSION

ATO and radiation had a synergistic apoptotic effect on GBM cells by up-regulation of caspase-3 and alteration of the Bax-Bcl-2 balance; therefore, ATO may act as a potential anti-cancer agent against GBM cells through triggering the mitochondrial pathway of apoptosis.

摘要

背景

三氧化二砷（ATO）已被报道为一种有效的抗癌药物，并且是美国食品药品监督管理局（FDA）批准用于治疗某些癌症的药物。本研究的目的是确定在多形性胶质母细胞瘤（GBM）细胞系U87MG中，在有或无电离辐射（IR）的情况下，ATO潜在的凋亡分子和细胞机制。

方法

细胞在有或无IR的情况下用不同浓度的ATO处理。使用MTT法评估处理组和对照组的活力和凋亡途径，并分别分析Bax、Bcl-2和caspase-3基因的表达。所有处理均在直径为100μm的球体上进行。

结果

结果显示所有处理组细胞的存活率均显著降低。正如预期的那样，联合治疗组的细胞存活率远低于仅用ATO治疗的组。此外，联合治疗使Bax和caspase-3上调，Bcl-2下调。

结论

ATO和辐射通过上调caspase-3和改变Bax-Bcl-2平衡对GBM细胞具有协同凋亡作用；因此，ATO可能通过触发凋亡的线粒体途径，作为一种潜在的抗GBM细胞的抗癌药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/5396e7b58149/IBJ-21-330-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/85c3b2273ad2/IBJ-21-330-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/98b9e7403cb8/IBJ-21-330-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/f69dfcbffad7/IBJ-21-330-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/28b6fb2bb208/IBJ-21-330-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/0e60fd98aa20/IBJ-21-330-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/5396e7b58149/IBJ-21-330-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/85c3b2273ad2/IBJ-21-330-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/98b9e7403cb8/IBJ-21-330-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/f69dfcbffad7/IBJ-21-330-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/28b6fb2bb208/IBJ-21-330-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/0e60fd98aa20/IBJ-21-330-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e23a/5548965/5396e7b58149/IBJ-21-330-g006.jpg

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